Since November 17, 1995, we have recruited 70 patients into our ongoing study. This particular project is concerned with identifying the influence of stroke on cardiac outcome. Patients have been assessed at one month, three months, nine months and twelve months following their stroke and this has necessitated their admission to the GCRC on Osler 5. When admitted, they receive a full clinical cardiological and neurological assessment together with a neurological score, a chest x-ray, an ECG, late potential evaluations, as well as assessment with a specially constructed platform which accrues one hour of data for assessment of heart rate, blood pressure and respiratory variability. In addition, a number of biochemical and hemorheological assessments are made in these patients. To date, we have an approximately 16% attrition rate, meaning that 16% of all the enrolled patients have been lost from the study. It is a fundamental feature of the statistical design of this study that we do not interrogate our endpoints which correlate cardiological outcomes with stroke location until the end of the study, which will be in four years time. However, we are interrogating the database for other stroke related data. For example, we have identified that approximately 15-20% of our patients who were thought to have lacunar infarctions on the basis of hypertension, have significant underlying structural cardiac disease suggesting that this is the etiology of their lacune. Principle amongst these is the presence of a fresh, mobile clot in the left atrial appendage. These data are being evaluated currently for communication at a subsequent clinical meeting. In addition, we have identified a new phenomenon which we have termed "the neurogenic stunned myocardium". These are patients who have no evidence of coronary artery disease, either from clinical examination or on history or on adenosine thallium scanning; however, they have evidence of either focal or global dyskinesias which cannot be explained easily on the basis of underlying coronary artery disease or diabetes. These data will be communicated at the forthcoming American Heart Association International Joint Conference on Stroke and Cerebral Circulation in February 1997. This phenomenon is important because it indicates a possible connection between the brain and the heart other than by influencing the coronary circulation. As such, it agrees with our previous animal experimental work which suggests that lesions in certain parts of the brain may alter cardiac autonomic balance, shifting it towards increased sympathetic drive. This increased sympathetic output can directly result in damage to the myocardium, structural damage, and reduced contractility. We are also monitoring CPK- MB levels in these patients to see whether there is specific evidence for damage to the cardiac musculature.